Fourth, the time from last scan to explant was <30 days, an acceptable time when imaging is reflective of pathology. There are weaknesses. Although the study is limited by sample size, finding clinical trial candidates being bridged to transplant, with solitary lesions

(most in our study had solitary lesions strengthening the analysis), and eligible for both Y90 and sorafenib (randomized trial) is extremely challenging. Second, we did not identify any effect of sorafenib on imaging or pathology; this may have been because of the relatively small size of the tumors. Reports of sorafenib decreasing enhancement and vascularity are usually illustrated in advanced selleck chemicals disease (infiltrative or large tumors, ± vascular invasion). Z-VAD-FMK Third, it was clear that, given the irregularity of tumoral enhancement posttreatment, there was a subjective element to measuring the longest enhancing tissue; these may be improved with (semi-) automated volume software. Fourth, whereas we observed that CPN could not be predicted by WHO and RECIST response classifications, we observed that smaller lesions were nevertheless more likely to exhibit CPN at explant. This is explained by the fact that measurement of treatment response by size

criteria (ignoring enhancement) almost never reaches zero; there is always a measurable defect after treatment. Finally, none of the imaging parameters evaluated Ergoloid in our study, including EASL and mRECIST, could reliably detect CPN at a microscopic level, highlighting the limitations of imaging methodologies that, despite being advocated by HCC guidelines, remain imperfect. On a tumor-by-tumor analysis, the adjunct of sorafenib to Y90 for HCC does not augment radio- or pathological response to therapy in HCC patients being bridged to transplantation. A reduction in standard size criteria (WHO and RECIST) at 1 month and a significant

reduction in enhancing tumor at 1 and 3 months was observed, but failed to reach significance, likely a result of the cytotoxic effect of Y90. Response to treatment was equivalent when measuring by EASL or mRECIST, neither of which could reliably detect CPN. A trend of smaller lesions at baseline (35-mm cutoff) was predictive of CPN. Diffusion-weighted imaging (ADC) did not change after treatment. Standardization of ADC measurements, automated volumetric software (measurement enhancing portions of tumors), and the combination of response criteria (anatomic plus functional) should be considered as future areas of research to improve the detection of CPN. Additional Supporting Information may be found in the online version of this article. “
“Recent progress in understanding the molecular mechanisms of bile formation and cholestasis have led to new insights into the pathogenesis of drug-induced cholestasis.